PMID- 27209071
OWN - NLM
STAT- MEDLINE
DCOM- 20170215
LR  - 20220409
IS  - 1840-4812 (Electronic)
IS  - 1512-8601 (Print)
IS  - 1512-8601 (Linking)
VI  - 16
IP  - 3
DP  - 2016 Aug 2
TI  - Apoptosis in pancreatic beta-islet cells in Type 2 diabetes.
PG  - 162-79
LID - 10.17305/bjbms.2016.919 [doi]
AB  - Apoptosis plays important roles in the pathophysiology of Type 2 diabetes 
      mellitus (T2DM). The etiology of T2DM is multifactorial, including 
      obesity-associated insulin resistance, defective insulin secretion, and loss of 
      beta-cell mass through beta-cell apoptosis. beta-cell apoptosis is mediated through a 
      milliard of caspase family cascade machinery in T2DM. The glucose-induced insulin 
      secretion is the principle pathophysiology of diabetes and insufficient insulin 
      secretion results in chronic hyperglycemia, diabetes. Recently, 
      hyperglycemia-induced beta-cell apoptosis has been extensively studied on the 
      balance of pro-apoptotic Bcl-2 proteins (Bad, Bid, Bik, and Bax) and 
      anti-apoptotic Bcl family (Bcl-2 and Bcl-xL) toward apoptosis in vitro isolated 
      islets and insulinoma cell culture. Apoptosis can only occur when the 
      concentration of pro-apoptotic Bcl-2 exceeds that of anti-apoptotic proteins at 
      the mitochondrial membrane of the intrinsic pathway. A bulk of recent research on 
      hyperglycemia-induced apoptosis on beta-cells unveiled complex details on glucose 
      toxicity on beta-cells in molecular levels coupled with cell membrane potential by 
      adenosine triphosphate generation through K+ channel closure, opening Ca2+ 
      channel and plasma membrane depolarization. Furthermore, animal models using 
      knockout mice will shed light on the basic understanding of the pathophysiology 
      of diabetes as a glucose metabolic disease complex, on the balance of 
      anti-apoptotic Bcl family and pro-apoptotic genes. The cumulative knowledge will 
      provide a better understanding of glucose metabolism at a molecular level and 
      will lead to eventual prevention and therapeutic application for T2DM with 
      improving medications.
FAU - Tomita, Tatsuo
AU  - Tomita T
AD  - Oregon Health and Science University. tomitat39@gmail.com.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20160522
PL  - Bosnia and Herzegovina
TA  - Bosn J Basic Med Sci
JT  - Bosnian journal of basic medical sciences
JID - 101200947
RN  - 0 (Apoptosis Regulatory Proteins)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - Apoptosis Regulatory Proteins/genetics
MH  - Diabetes Mellitus, Type 2/genetics/*pathology
MH  - Humans
MH  - Insulin Resistance
MH  - Insulin-Secreting Cells/*pathology
MH  - Mice
PMC - PMC4978108
EDAT- 2016/05/23 06:00
MHDA- 2017/02/16 06:00
PMCR- 2016/08/01
CRDT- 2016/05/23 06:00
PHST- 2015/12/01 00:00 [received]
PHST- 2016/01/20 00:00 [accepted]
PHST- 2016/01/16 00:00 [revised]
PHST- 2016/05/23 06:00 [entrez]
PHST- 2016/05/23 06:00 [pubmed]
PHST- 2017/02/16 06:00 [medline]
PHST- 2016/08/01 00:00 [pmc-release]
AID - BJBMS-16-162 [pii]
AID - 10.17305/bjbms.2016.919 [doi]
PST - ppublish
SO  - Bosn J Basic Med Sci. 2016 Aug 2;16(3):162-79. doi: 10.17305/bjbms.2016.919. Epub 
      2016 May 22.